The harmful health effects of lead have been known for thousands of years,
but observations of injurious effects at low levels of lead have been the
subject of increasing concern in the past few years. Recent research has pointed
to possible dangers faced by specific populations who risk lead exposure from
mobilization of their body lead stores, e.g., children, pregnant women and
osteoporotics. Lead toxicity is reported to be a major public health problem in
the United States today. The general population is exposed to lead in their
environment. This lead can come from several sources, e.g., house paint, water
and soil. Although lead has been banned from house paint, older housing stock
still contains lead paint which can contaminate household dust. Lead was removed
from American gasoline in the early 1980s, and lead levels in children has
fallen considerably. Yet this previous use has resulted in soil contamination
which still exists. Lead continues in use in many plumbing fittings. Many areas
still receive their water supply through lead pipes. All of these factors can
lead to an elevated total lead consumption.

Environmental exposure to lead is not the only source of lead-related health
effects. Many industrial workers in the United States have potential
occupational exposure to lead, and lead poisoning is still seen at occupational
health clinics.

Clinical lead poisoning in itself does not define the extent of lead-related
health problems. Recent research has shown that increased lead exposure, even at
legally permissible levels, can lead to harmful, though sub-clinical, effects.
Some of the earliest symptoms of the ailment are non-specific, such as fatigue
and muscle pain and are frequently ascribed to factors other than lead
poisoning. Other effects include changes in kidney function, inhibited central
nervous system function and reduced nerve conduction velocity, the latter having
been demonstrated in lead workers who showed no symptoms. This means that more
adults may be affected by both environmental and occupational lead exposure than
can be estimated from the numbers who present at clinics.

At the present time, exposure to lead is most commonly monitored by measuring
blood-lead levels. The criteria for lead poisoning and lead toxicity are based
on blood-lead as a standard. However, the biological half-life of lead in blood
is approximately 36 days. It is therefore an indicator only of recent lead
exposure. Blood-lead reflects chronic exposure only if exposure is constant and
the measurements were constant and well documented. Deleterious health effects
of lead resulting from long-term lead exposure will only be correlated with
current blood-lead levels if lead exposure has been relatively constant over a
long period of time, up to the time of sampling.

Measuring lead in blood has methodological drawbacks and limits on
physiological interpretation. Methodologically, measuring lead in blood
frequently requires a venous sample and sending blood to a laboratory for
analysis. In most states, the delay between sampling and analytic results can be
6-8 weeks. This delay obviously impedes efficient public health prevention,
since in the absence of immediate feedback no decision can be made on risk
reduction at the time of initial screening or clinic visit. Often, it is
difficult to locate the persons who were sampled after this delay, and, of
course, exposures may continue in the interval. Physiologically, the measurement
of lead in blood is not a direct assessment of target organ dose, since the red
cell is not a critical target for lead toxicity. Kinetically, blood is not a
good analog for critical targets, such as soft tissue, because of the relatively
short half-life of lead in blood as compared to target organs or bone.

Long-term lead exposure is of primary health concern but can rarely be
ascertained from blood-lead records. No one in the general population has an
adequate blood-lead measurement history. However, 109Cd K X-Ray
Fluorescence (XRF) bone-lead measurements allow the direct measurement of
long-term lead exposure.

At the present time, little is known about the range of chronic environmental
exposures in the general population. Further research is required for the full
implications of chronic lead exposure to be thoroughly understood. However, 109Cd
K XRF bone-lead measurements have the potential to enhance our understanding of
the effects of low-level lead exposure and consequently to determine whether the
current intervention criteria, which are based on blood-lead levels, afford
adequate protection against the effects of lead. Bone-lead measurements may also
provide an additional screening technique in the identification of high-risk
populations.

Lead is predominantly stored in the human body in calcified tissues; 90-95%
of the total lead burden is contained within bone in non-occupationally exposed
adults. The total lead content of bone is reported to be up to 200 mg in 60-70
year old men, less in women. The turnover rate of lead in cortical and
trabecular bone is slow; quantitative estimates of the half-life vary, but there
is a consensus that it is of the order of years or even decades. Therefore,
through childhood and most of adult life, lead exposure from both environmental
and occupational sources results in an increased lead concentration within the
bone matrix. A measure of bone-lead content thus reflects integrated or
cumulative, and thus long-term or chronic, lead exposure and provides a useful
surrogate indicator of the cumulative dose of lead presented over time to the
target organs of lead.

In vivo bone-lead measurements may therefore clarify the risks associated
with lead exposure in two ways. Health effects which are associated with chronic
lead exposure may be identified by their correlation with bone-lead level, and
bone-lead measurements may ultimately allow the identification of subjects at
risk from mobilization of their body lead stores and allow appropriate
intervention strategies to be devised.

Under conditions where bone physiology is undergoing a period of change, such
as during pregnancy, aging and osteoporosis, it would appear that lead can be
released from the bone mineral matrix, increasing blood-lead levels and
constituting a further source of lead exposure. It would seem likely that the
level of this endogenous exposure would be dependent on bone-lead burden.

Several large in vivo studies have confirmed that the integrated 109Cd
K XRF bone-lead measurement is a measure of long-term lead exposure. Bone-lead
measurements have been performed on more than 800 occupationally exposed workers
in England, Sweden and Finland in several studies. The occupationally exposed
groups were studied as extensive blood-lead records were available on these
subjects; in some cases records extended as far back as 1950. It was found in
all the individual studies that bone-lead level of all bone sites including the
tibia, calcaneus and sternum, correlated with the "Cumulative Blood-lead
Index" (CBLI). The CBLI is an integrated time-weighted average blood-lead
level and thus corresponds to total lead exposure. The studies reported that 109Cd
K XRF bone-lead measurements could therefore be considered to be a measure of
cumulative lead exposure.

Evidence therefore exists that the 109Cd K XRF method can provide
an accurate measurement of bone-lead level, to well within the currently
available levels of precision, and further that this measurement of lead in bone
can be considered to be a measure of long-term lead exposure.

The radiation dose and consequent risk arising from a K XRF bone-lead
measurement are very small for all age groups, including children.